Flashcards in Endocrine Diabetes and Metabolism UWorld Deck (93)
Thyroid nodule aspirated to show large overlapping nuclei with finely dispersed chromatin, numerous intracellular inclusions and grooves and psammoma bodies.
Papillary thyroid carcinoma demonstrates cells with a ground-glass appearance and Orphan Annie nuclei
Thyroid nodule aspirated to show marked pleomorphism, irregular giant cells and basophilic spindle cells.
Anaplastic thyroid carcinoma.
Thyroid nodule aspirated to show polygonal spindle-shaped cells with a slightly granular cytoplasm and adjacent amyloid deposits
Medullary thyroid carcinoma
Levels of anti-androgen therapy
GnRH agonist - leuprolide
Inhibition of testosterone synthesis by Leydig cells - spironolactone
Inhibition of 5-alpha reductase: finasteride
Antagonism of androgen-binding receptor: flutamide, cyproterone and spironolactone.
PTH and Ca in primary and secondary hyperparathyroidism
Primary: both elevated
Secondary: PTH elevated, Ca low
Note that diuretics, vitamin D intoxication, granulomatous disease and lymphoma will cause an elevated Ca with low PTH.
How does thyroid hormone get synthesized?
I- is transported via the Na/I symporter against its gradient
Inside the follicular cells, I- undergoes organification to I2 by the enzyme thyroid peroxidase.
It then binds tyrosine residues on thyroglobulin to form MIT. 2 MITs can join together to form one DIT. 2 DITs can join to form T4 and a DIT + MIT can join to form T3.
In the thyroid cytoplasm, thyroglobulin is separated from the iodinated tyrosine residues that get secreted as T3 and T4. Inactive MIT and DIT residues are then recycled.
How do glucocorticoids cause adrenal atrophy?
They suppress CRH release from the hypothalamus and reduce the effect CRH has on the anterior pituitary. This causes atrophy of the CRH-secreting neurons in the hypothalamus, atrophy of corticotrophs in the anterior pituitary and atrophy of the adrenal gland.
Pioglitazone mechanism of action
It is a thiozoladinedione that binds PPAR-gamma which causes it to form a heterodimer with the retinoid X receptor. This results in increased GLUT-4 production (increasing insulin sensitivity), increased adiponectin (increases the number of insulin responsive adipocytes and up regulates beta-oxidation) and decreased production of TNF-alpha and leptin.
Delayed puberty + anosmia
Kallman syndrome: failure of the GnRH secreting neurons to migrate from their olfactory placode due to mutation in KAL-1 or FGFR-1 genes.
How does insulin affect glycolysis
It increases the activity of PFK-2, which converts Fru-6-P to Fru-2,6-BP. In turn Fru-2,6-BP activates PFK-1 and inactivates Fru-1,6-bisophosphatase, promoting glycolysis and inhibiting gluconeogenesis.
Note that glucagon activates Fru-2,6-bisphosophatase, reducing the amount of Fru-2,6-BP and promoting gluconeogenesis.
Inhibitors of thyroid hormone synthesis
PTU + Methimazole: inhibit thyroid peroxidase and prevent the organification of iodine and its coupling to tyrosine
Excess iodide: Wolff-Chaikoff effect, temporarily inhibits TPO and I- uptake...this is why you give KI if people are exposed to radioactive I131
Perchlorate and pertechnetate: inhibits I- transport through Na/I symporter
PTU, beta-blockers, ipodate: inhibit peripheral conversion of T4 -> T3 by inhibiting 5' deiodinase
Hormones that signal through G-protein coupled receptor that activates adenylate cyclase.
Hormones that signal through G-protein coupled receptor that activates guanylate cyclase
ANP, BNP, NO
Hormones that signal through intrinsic tyrosine kinase activation
Insulin + growth factors
Hormones that signal through JAK/STAT tyrosine kinase activation
Hormones that signal by binding an intracellular receptor
Hormones that signal through G-protein coupled receptor that activates phospholipase C -> DAG + IP3 formation
Muscles innervated by the superior laryngeal nerve and recurrent laryngeal nerve
Superior laryngeal has two branches: external and internal
-External: only innervates the cricopharyngeus and is prone to injury as it lies directly beneath the superior thyroid artery
-Internal: sensation to mucosa above vocal cords
Recurrent laryngeal: posterior and lateral crycoarytenoids, oblique and transverse arytenoids and thyroarytenoid
Effects of insulin on the cell after binding to its transmembrane surface receptor
Activation of cytosolic tyrosine kinase -> protein phosphatase activation -> glycogen synthase and fructose-1,6-bisphosphatase, dephosphorylation leading to activation of glycogenesis and deactivation of gluconeogenesis, respectively.
Disorganized lamellar bone structure in a mosaic pattern
Excessive osteoid matrix accumulation around trabeculae
Vitamin D deficiency
Persistence of primary spongiosa in medullary cavity without mature trabeculae
3 presentations seen in 21-hydroxylase deficiency
Classic, salt-wasting: girls with ambiguous genitalia and hypo-aldosteronism at birth
Classic non-salt wasting: girls with ambiguous genitalia at birth, boys with virilization around 2-4
Non-classic: precocious puberty, acne, hirsutism
Treatment of CAH
Low exogenous doses of corticosteroids to suppress ACTH release
Location of genes that code for rRNA and tRNA needed in mitochondrial protein synthesis
Compound that gets converted into vitamin D3 (cholecalciferol) in the skin
Patient has diabetes and erythematous plaques and papules on his legs, arms, face and perineum. As time goes on they enlarge and coalesce to have a central bronze-colored area with peripheral blistering and scaling.
This patient has necrolytic migratory erythema and diabetes suggestive of a glucagonoma.
Infant with marked cardiomegaly, hypotonia, macroglossia and hepatomegaly with normal glucose levels and muscle biopsy showing glycogen within lysosomes
Acid alpha-glucosidase, resulting in Pompe disease. The glycogen inside lysosomes is particularly specific for this disease.
Biologically active form of pantothenic acid